Size Difference
The size of tympanic membrane is 0.9 centimeters square, but only the pars tensa portion plays a role in sound transmission, and that area is 0.59 centimeters square. The size of the stapes footplate is 0.032 centimeters square. So you have reduction in size.
There’s a 18.6 difference between the pars tensa part of the TM(tympanic membrane) and stapes footplate. The pressure formula consists of a certain amount of force being applied to a small area (like the stapes) resulting in an increase of pressure.
There’ll be a 18.6 fold increase in pressure by the time the energy reaches the oval window, since the same force is being applied to a smaller area. (Remember, Pressure = Force/Area). This will translate into a 25 dB boost in amplification or a 1000 Hz gain(frequency that our ears are most sensitive to).

Describe the second component of middle ear transformer action?

Transformer Action of Middle Ear - Lever Action (Fulcrum effect)

NOTES:

Slide 10: Lever Effect
When there is a large person on one end and a smaller person on the other end of the see-saw, the fulcrum must be adjusted so the smaller person will be able to lift the heavier person. The basis of the lever effect is that a little pressure generates a greater force on the opposite ear.

What are the 3 components of the lever action of the middle ear?

Involves:

1. fulcrum location
2. manubrium of malleus
3. long process of incus

NOTES:

The manubrium of the malleus(pressure on left side of the fulcrum) is about 1.3 times longer than the long process of the incus(heavy mass on right side of the fulcrum). Straightening the fulcrum will result in an increase pressure at the footplate of the stapes, resulting in an resulting in gain of about 3 dB gain.
The total gain from the tympanic membrane to the stapes footplate (25 dB) and the lever action (3dB) is about 28 dB.

How do you measure the amount of amplification based on transformer action?

 The manubrium of the malleus(pressure on left side of the fulcrum) is about 1.3 times longer than the long process of the incus(heavy mass on right side of the fulcrum). Straightening the fulcrum will result in an increase pressure at the footplate of the stapes, resulting in an resulting in gain of about 3 dB gain.

 The total gain from the tympanic membrane to the stapes footplate (25 dB) and the lever action (3dB) is about 28 dB.

Describe the minimum audibility curve and its 2 major characteristics?

1. It reflects sensitivity of ear in dB as a function of frequency.

2. The shape of the curve is due to transformer action of middle ear

NOTES:

 You lose about 97 %, and you gain about 60 % of the incoming sound in your ear. A 100 % gain is not good, since it will disrupt important sounds(speech), since you will hear too much(mouth moving, heartbeat). The sound gain is specific for each species(speech oriented for humans, survival oriented for other animals).

 The chart shows threshold of listening. They kept increasing the frequency(control) on the X-axis until the threshold was at its lowest.

 On the chart, the y-axis the sound level, and the x-axis is the frequency. 140 dB is the threshold of pain. In terms of the human we hear from 20 to 20000 Hz. Frequency below 20 Hz is infrasonic, and frequency above 20,000 Hz is ultrasonic.

 Soft consonants are high frequency sounds and the vowels are low frequency sounds. Our hearing is most sensitive at 1000 Hz to 4000 Hz.

 The minimum audibility curve shape is due to the shape of the transformer action of middle ear . In the upper limits there is the threshold of pain is 140 dB.

What is an audiogram?

An audiogram is a diagramatic representation of someone’s hearing’s threshold. We test from 125 Hz to 8000 Hz because that’s where the speech range falls. Between -10 and 20 dB is normal.

1. Normal hearing
0-20 dB HL
2. Mild loss
25-40 dB HL

3. Moderate loss
45-60 dB HL

4. Severe loss
65-80 dB HL

5. Profound loss
> 80 dB HL

Describe the traveling wave phenomenon?

TRAVELING WAVE PHENOMENON – The cochlea is tonotopically organized due to the gradation mentioned above. The basilar moves like a traveling wave that crests at 7000HZ. Then the membrane moves vigorously. Then the thing will dissipate. This then continues to cause movement to the apex. On the low freq sound: the fibers are at the apical cochlea. Then the crest occurs at apex, in the vicinity where the reference frequency matches the incoming signal. Causes the displacement of the organ of cori, on the basilar mem. This is the tonotopcal org that begins in the cochlea and involves basilar membrane.
1. Basilar membrane moves in the form of a traveling wave
2. Cochlea is tonotopically organized

NOTES:

 A high frequency sound will move in the basilar membrane in the form of a traveling wave. Each basilar fiber has its own resonance characteristics. The crest of the traveling wave will be in the same location where the basilar fibers have the same resonance frequency as the incoming sound.

 Traveling wave always goes from base to apex. Therefore, a high frequency sound will travel through the outer ear, through the middle ear, through the basilar membrane and the energy of that sound will be used whenever its frequency matches the resonance frequency of the basilar membrane, and its energy will be dissipated at the basal end of the cochlea.

 On the other hand, a low frequency sound will travel and dissipate its energy at the apical end of the cochlea.

Illustrate the organization of the organ of corti and its 5 major components?

It is the Sensory end organ of hearing!
Slide 20: Organ of Corti
The tectorial membrane is above the organ of Corti. Receptor cells, inner and outer hair cells are visible. The longest cilia of the outer hair cell is imbedded in the tectorial membrane. The inner hair cell is not imbedded in the tectorial membrane.

Two types of receptor cells found in the cochlea: outer hair cells and inner hair cells. Outer hair cells have 3 to 5 cells, inner hair cells have one row. Outer hair cells have a long stereocilium embedded in the tectorial membrane, inner cells don’t have that. Outer hair cells are cylindrical in shape, inner hair cells are flask-like in shape, and the differences go on and on.

The reticular lamina is made up of the tops of the rods of Corti, the ditter cells are one of the supporting cells for the outer hair cells, and they have the tops of the phalyngeal process that make up part of the reticular lamina. The cuticular plates of the hair cells also make up part of the reticular lamina.

Collectively they form a tight junction that separates the endolymphatic fluid in the scala media that bathes the hair cells through the tunnel of Corti, which has perilymph inside it. To summarize, the tops of the phalyngeal processes of the ditters, the tops of the rods of Corti, the cuticular plates of the hair cells make up the reticular lamina.

Describe the functional morphology of hair cells and name the motor protein involved in their action?

The molecular mechanism for this action involves the motor protein 'prestin', and is able to contract the cell by up to 10% of its length [5,6]. See [7,8] for more information regarding this motor molecule. The outer hair cells receive little afferent innervation, and are therefore believed to play little role in directly transducing sound stimuli to the brain. The motile capabilities of these cells suggest that they may play a role in adjusting the motion of the basilar membrane and affecting the amplitude of stimulation received by the inner hair cells; the outer hair cells might play a role in the amplification of weak stimuli - the so called 'cochlear amplifier'

Describe the resting membrane potential of different parts of the cochlea?

 If you were to put an electrode lead in the scala typani(point of reference) and another lead in the scala media, it will register + 80 mV. Therefore, the scala media has a resting potential of +80 mV. The outer hair cells have a resting potential of - 70 mV, and inner hair cells have a resting potential of -45 mV, relative to the scala tympani. The scala vestibuli should have no resting potential difference, since the liquid that flows through the scala vestibule and the scala tympani are the same. However there is a little voltage difference of 2 to 5 mV. The scala tympani has a resting potential of 0 mV with respect to itself.

Describe the role of these in ionic channels and potassium diffusion:

1. tip links
2. cross links
3. cuticular plates

They are protein linkages involved in stretching and compressing.

1. tip links: connect shorter and longer stereocilia within each row of a bundle

2. cross links: connect stereocilia of different rows, within each bundle even down to the rootlets

 When the bending is towards the longest stereocilium, the tip links are stretched, then it opens up the potassium channels. The fluid here is the endolymph.

Describe the exact role of potassium in neurotransmitter release or inhibition?

Like the endolymph, the intracellular fluid is also high in K+ and low in Na, but there’s a more potassium in the endolymph than in the cell, so potassium will diffuse inside the cell (from high conc. to low conc.), depolarizing the cell, allowing calcium to come in. Vesicles in the cell will then bind to the membrane, releasing neurotransmitters into the synaptic cleft.
When the bending (fluid here is the perilymph, which is high in sodium, low in potassium)is away from the longest stereocilium, the tip links are compressed, and the potassium will diffuse from inside the cell towards the outside the cell, causing hyperpolarization.

1. In the inner hair cells, a low frequency tone (300) will induce an oscillating alternating (AC) current, constituted of alternating depolarizations and hyperpolarizations. If you increase the current (500,700, 900), the oscillations increase and the amplitude decreases. When you continue to raise the frequency of the input (5000 Hz), you see a baseline shift( constant depolarizing DC current), with minimal AC potential.

2. Outer hair cells with a low frequency stimulus will produce a large AC and a depolarizing DC, but with a high frequency stimulus will produce attenuated AC and DC.

Differentiate between the 2 types of extracellular receptor potentials?

If you were to introduce a sound to the ear, you are using tuning curves to determine when the auditory nerve fiber begins to fire above the spontaneous rate. The intensity that it just begins to fire above its spontaneous rate is the threshold response of the auditory nerve fibers.
- At 1000 Hz, it begins to fire above its spontaneous rate at 20 dB, for example.

-You then determine the spontaneous rate at different frequencies, and connect the dots on the graph. For this particular chart, it is evaluated at the characteristic frequency(lowest threshold response) at 1000 Hz. The characteristic frequency is the frequency that auditory nerve fiber responds best, and it is located at the basal end on this chart (remember, the basal end is the region that encodes high frequencies.

-The auditory nerve fiber also responds to other frequencies above and below its characteristic frequency, but at a higher intensity.

-The width of the tip indicates how fine-tuned the auditory nerve fiber is. The wider the tip, the less fined tuned it is, the narrower the tip, the more sharply tuned it is.

- The auditory nerve fibers that innervate the basal end of the cochlea have high characteristic frequencies with long tails.
- The auditory nerve fibers that innervate the apical end of the cochlea have low characteristic frequencies and are “V” shaped.
- The lower frequency region (apical end) is not as finely tuned as the higher frequency region (basal end).

The traveling wave is going from base (high frequency) to apex (low frequency). However, the tuning curve goes from low frequency to high frequency. Both auditory nerve fibers have high characteristic frequencies on this chart. Therefore, they will innervate the basal end of the cochlea.

-An animal with the normal auditory nerve fiber was given kanamycin, which damages the outer hair cells in the cochlea. The threshold is way elevated with the damaged auditory nerve fiber, with the tip now located at a much lower frequency. The tip is broader and now elevated, which means it is now less fine-tuned.

-Although kanamycin doesn’t damage the auditory nerve fiber; the auditory nerve fiber is still affected. Ototoxic drugs such as kanamycin will damage the outer hair cells, resulting in hearing loss.

hOT BELl

If only 5% of ANF innervate Outer Hair Cells and Ototoxic drugs damage Outer Hair Cells, why would there be a significant Hearing Loss due to ototoxic drug?
Describe this paradox of ototoxic drugs?

It must be something Outer Hair Cells are contributing to the process that once gone results in Hearing Loss.  95 % of auditory nerve fibers innervate the inner hair cells., and only 5 % innervate the outer hair cells. And although the 8th cranial nerve is intact, the damage causes broad tuning of the 8th cranial nerve.

What are 3 characteristics of Outer Hair Cells?

1. Contractile proteins found in OHCs stereocilia and throughout hair cell structure

NOTES:
You have the intense sound (60 dB or above) coming in, and it is strong enough to cause movement of the basilar membrane. If you have a strong sound coming in, then it’s going to cause the inner hair cells cilia, which are not embedded in the tectorial membrane, to bend. This results in the depolarization of the inner hair cells, which will release neurotransmitter unto the nerve fiber, subsequently generating an action potential.

 When you have a low intensity sound, the outer hair cells will be activated, changing the outer hair cells length, which will increase the amplitude, activating the inner hair cells.

NOTES 2:

. ACTIVE AND PASSIVE MECHANISM- low intensity sound may not allow enough movement for them to respond. They are insensitive. They have to have sufficient movement to activate them. Once the stimulus is strong enough, the cilia moves, depolarized NT onto the nerve to the brain then to the cortex, but you need a 60 db stimulus: 95% of the auditory nerve fibers innervate the ear. But otherwise they are not there. Low intensity  shearing cilia move longest area depolarized contract (away, hyper and elongation) movement goes higher then the inner hair cells make contact and trigger the process. THE OUTTER HAIR CELLS SERFVE AS HEARING AIDS FOR THEINER HAIR CELLS AND FACILITATE THE ABILITY FOT THE INNER HAIR CELLS TO HEAR. The distortion products go from cochlea to the ear  to acoustic emissions. This tells us about the outer hair cells of the cochlea. This is how you screen the newborn

Describe OTOACOUSTIC EMISSIONS?

It is used to screen for hearing loss.
OTOACOUSTIC EMISSIONS- newborn screenings: they are very low intensity sounds. Picking them up tells us that the child hears sounds. The most sensitive is the outer hair cells. OAE rules out the hearing loss. The baby can be deaf and still have OAE if the nerve is damaged. OAE is only a test for the cochlear function. Nerve is the auditory neuropathy.
When the cochlea gets damaged, the Outer hair cells get damaged first, then, with continued exposure, the inner hair cells get damaged. The cochlea is susceptible to noise damage (hair dryer, car stereo, clubbing). Right after returning from a loud concert, one may get temporary threshold shift (difficulty in hearing result right after the event).

Discuss the effects of Inner ear lesions (hearing loss) on OHCs and IHCs?

-Hearing loss type:
sensorineural

-Hearing loss severity:
ranges from mild to profound

1. OHC damage
-loss of volume
-Loss of frequency selectivity: ability to separate sounds of different frequencies is compromised

2. IHC damage
-loss of volume
-Loss of clarity

NOTES:

 Damage to the inner ear results in sensorineural hearing loss. two types of hearing loss. Outer cells loss results in a loss of volume, and they get damaged first. Continual damage results in inner hair cell loss, and that results in loss of clarity. It has impact on a person’s ability to follow conversation.

NOTES:
Frequency Theory: This theory states that the frequency is the number of times the nerve fibers fire that encode frequency. The problem is that the frequency is limited to 1000 Hz, since that’s the highest frequency a nerve fiber can reach

Describe volley theory?

-Suggests that many nerve fibers contribute to frequency encoding by firing in rapid succession

-Problem: Can only account for frequencies up to 6000 Hz

NOTES;
 This theory suggest that many nerve fibers firing asynchronously, but the highest frequency that can be reached is 6000 Hz.

Describe the place theory?

-Suggests the place along basilar membrane encodes frequency
-Limitation: Can only account for frequencies above 5000 Hz

NOTES:

This suggest that it’s the place along the basilar membrane that encodes frequency(remember, the basilar end is finely tuned as opposed to the apical end). It holds true for frequencies above 5000 Hz, but not below 5000 Hz.

Describe the place - volley theory?

It combines place and volley theory:
-Place theory accounts for High Frequency hearing

-Volley theory accounts for Low Frequency hearing

NOTES:
 This theory combines the place theory (place along the basilar membrane) and the volley theory(many neurofibers firing asynchronously).

Describe intensity encoding?

Spike rate of one Afferent Nerve Fiber (ANF) as a function of stimulus level

NOTES:
INTENSITY ENCODING – hear from 0 to the 140 db in the pain threashold. Increase the intensity and you increase the spike rate to a point to a range of about 30 db. Our range goes out to 140.

What does this illustrate?

The concept of intensity encoding, illustrating the Spike rate of one ANF at different intensities and frequencies.  You want to know the dynamic range of the auditory nerve fibers. As the intensity increases, the spike rate increases, and then it plateaus, so one auditory nerve fiber cannot be responsible for the wide range of intensity range that we have.

What does this show?

Response of many ANFs as function of intensity
– the characteristic freq (CF) is where it discharges the most. The boost at the 10 DB will show a boost at different ranges. At some point it discharges. So the freq is coded by the collective response. As you increase the intensity, you recruit more and more nerve fibers. So you do all of that s well as the intensity of the neural discharge.

Intensity encoding involves what 2 things?

1. Discharge pattern of a given ANF

2. Density of neural discharge

Describe the 2 middle ear muscles?

1. STAPEDIUS MUSCLE:
-The tendon of the stapedius muscle comes into the middle ear space and attaches to the neck of the stapes.
- When the stapedius muscle contracts as a result to noise (60-90 dB above threshold) it pulls the stapes laterally and posteriorly, making the movement of the ossicular chain less efficient.
- The stapedius muscle have minimal attenuation(5-10 dB), regardless of frequency, as long as the noise is 60-90 dB threshold. That muscle does not attenuated high frequency noise above 1000 Hz.
- The stapedius muscle is innervated by cranial nerve 7.

2. TENSOR TYMPANI MUSCLE:
- The tendon of the tensor tympani attaches to the manubrium of the malleus, and when it contracts, it pulls manubrium medially.
-
 Both muscle stiffen the tympani membrane, so more sound reflects off the tympanic membrane, and less sound passes through the system, protecting the ear from loud sound.
-tensor tympani muscle is innervated by cranial nerve 5.

EXTRA NOTES:
Stampedius muscle – nerve 7 this contracts when the sound is loud. This will stiffen the chain and more sound reflects of the eardrum thus protects from the loud sound. This can reflect from 5-30, but the average is 10db, and frq 1000 or below. High freq are not affected, but the low ones are. The high freq pass through, without stiffness mattering. TO DAMAGE YOUR HEARING YOU AVE TO HAVE ABOUT 120. if you leave, your ear rings and you don’t hear as well. that is too loud. This is not working efficiently to attenuate that. Once you reach 85 db for 8 hours. Every time your raise the DB by 5 you have to cut the time by half.

-The afferent component is the CN VIII. The sound comes in the CN VIII and synapses in the ventral cochlear nucleus. The second order neuron then passes through the ipsilateral motor nucleus of VII, which houses the cell bodies of the CN VII, which innervates the stapedius muscle, and then the muscle contracts.

-Any lesion in the facial nerve or CN VIII, will make the stapedius muscle unable to contract, since the neural information won’t reach it = hyperacusia.

Describe Right Facial Nerve Paralysis?

This results in bell's palsy, which is paralysis of the facial nerve producing distortion on one side of the face.

NOTES:
8th is the afferent, 7th is the efferent—Sound 8 cell bodies on the VCN MN of 7 cell bodies of the 7th CN stapedius muscle oipsilateral. The loud sound will trigger this and attenuate the low freq sound.
Lesion of he CN7 in bells palsy, stapedius will not contract. This is the bells palsy guy.

Describe the effect of CNVII Lesion Site on Stapedius Muscle?

 If the nerve compressed is lower or distal to the innervation of the stapedius muscle, then it will contract. If the nerve is above or proximal to that muscle, then it won’t contract.

NOTES

know if the depression is proximal or distal to the other ones. This shows the face. If the reflex goes off: it is distal. If it is above the innervations of stapedius, then the motot component that is involved.
Ipsilateral Pathway

Describe the Contralateral Stapedial Reflex Arc?

 Sound coming in goes through the ventral cochlear nucleus goes through both superior olive complexes, then it goes through both motor nucleus CN VII, and both stapedius muscles will contract. So you can stimulate one ear and trigger both reflexes because of this reflex pathway.

NOTES:
. this is the contralateral arc that is for the reflex. That is the bilateral representation. Output from both go to both the motor nuc 7. so if you intro a sound to one ear, both muscles contract.

What are the roles of the 5 components of the contralateral stapedial reflex arc?